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User:Robins3

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Phage Hunters Spring 2017

My Annotations

StatusPageDate/TimeGO Term (Aspect)ReferenceEvidenceNotesLinks
updatedbyinstructor9CAUD:W0TUZ22017-04-05 10:27:44 CDTGO:0098670 entry receptor-mediated virion attachment to host cell (P)PMID:27422842ECO:0000315 mutant phenotype evidence used in manual assertion

Figure 6. Takeuchi et al. found that 2 mutations, M103 and M20, in orf103 of phage ΦSA012 enhanced adsorption allowing infection of the normal ΦSA012-resistant organisms that they would otherwise not be able to infect. This was confirmed by adsorption assay and spot testing.

challenge
updatedbyinstructor9CAUD:W0TUZ22017-04-05 10:26:19 CDTGO:0098024 virus tail, fiber (C)PMID:27422842ECO:0000314 direct assay evidence used in manual assertion

Figure 5. Takeuchi et al. used gold-conjugated anti-orf103 antibodies known to specifically bind to the orf103 gene product. Gold-bound Ab allowed for visualization of the location via immunoelectron microscopy. They found that the gene product localized in the tail fiber at the bottom of the baseplate.

challenge
unacceptable9CAUD:W0TUZ22017-04-05 10:44:07 CDTGO:0098001 receptor-mediated bacteriophage reversible attachment to host cell (P)PMID:27422842ECO:0000315 mutant phenotype evidence used in manual assertion

Figures 2 and 3. Takeuchi et al. found that ΦSA012TM103 and ΦSA012TM20 mutant variants of ΦSA012 could not infect host RN4220. ΦSA012TM103 only produced turbid plaques when plated with RN4220 and ΦSA012TM20 could not produce plaques at all. The reason being that RN4220 has the tarM gene which produces α-GlcNAc modification of WTAs. With this modification ΦSA012 mutants cannot infect RN4220. RN4220 with tarM deleted became susceptible to both ΦSA012 mutants as shown in spot tests and adsorption assays.

challenge

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